Weak Immune System May Open Aids Door

Immune System Has Variety Of Weapons

To best comprehend the role played by other diseases in the attack by HIV, a brief and highly simplified tour of the human immune system is in order.

The immune system is the body`s defense against diseases, from the common cold to Lassa fever, and it encompases a variety of complex weapons, the most important of which are antibodies produced by the white blood cells.

Whenever an invading microbe breaches the body`s barrier defenses it is the cells that act as the forward scouts of the immune system, the

macrophages, that identify the enemy and report the invasion.

When a second cell, the helper T cell, receives notice the enemy is at hand, it begins to clone itself at a furious rate and to spew out chemicals, called lymphokines, that are the body`s signal to itself an invasion is underway.

If the helper T cells are the officers of the immune corps, the paratroops are the B cells. When the B cells receive the biochemical warnings sent by the helper T cells, they too become activated, increasing in size and reproducing themselves by dividing in half.

Now the B cell army, much enlarged, begins to fight the disease by producing yet another kind of chemical, called an antibody, that is the deadly enemy of this particular invader.

In the meantime, however, the enemy has dug in, invading some of the body`s other cells and using their genetic machinery to reproduce itself, polluting the bloodstream with ever-increasing numbers of freshly minted viruses.

But when their genetic material is exhausted, the invaded cells die, taking their invaders with them to the grave, while the antibodies being pumped into the bloodstream at the rate of thousands of molecules a minute seek out and attack the rear echelons of the enemy.

After a week or two of fever, chills and aches, the disease has been vanquished, but how is the immune system to know the war is over?

Left to their own devices the helper T cells would continue calling for reinforcements, sending ever-more B cells to the front to fight a nonexistent enemy.

Since the unfettered production of B cells, a condition known as lymphoma, is just as undesirable as the disease they were meant to destroy, a second kind of T cell now takes over the chain of command.

Known as the suppressor T cell, it also sends signals to the B cells and helper T cells. But these signals tell the other cells to relax and return to a dormant state while they await the next invasion.

That is how the immune system works in the case of an invasion by an ordinary virus. Unfortunately, HIV, the human immunodeficiency virus, is no ordinary virus.

Of the several kinds of cells that HIV chooses to turn into HIV-producing factories, its favorite are the same helper T cells that signal the beginning of an invasion and orchestrate the movement of the troops-the most crucial component of the entire immune system.

If the host has a full complement of T helper cells when the invasion begins, there may be enough of them to knock the virus down before it gains a foothold, or at least keep it under control.

But if the invading HIV molecule leaves a critical number of helper T cells damaged and dying, the body is left vulnerable to the kinds of

``opportunistic`` infections to which those with normal T cells counts are immune, but which for the immune-deficient are fatal.

They include a rare kind of pneumonia, a malignant tumor called Kaposi`s sarcoma, otherwise minor parasitic infections like cryptosporidosis and toxoplasmosis, even animal diseases like a bacterium that causes tuberculosis in birds.

Those whose immune systems are less severely compromised may go through an alternating cycle of illness and recovery, while for those with even more minor immune deficiencies, AIDS may be no worse than a bad case of the flu.

Whatever its final outcome, there appear to be several possible ways in which previous or concurrent infections can pave the way for these and other AIDS-related diseases.

Herpesviruses, for example, appear to stimulate the replication of HIV. Studies show that gay men with pre-existing herpesvirus infections are three to four times more likely to become infected with HIV, and that one herpesvirus, EBV, may provide the means for HIV to infect B cells as well as T cells.

Such infections also tend, over time, to cause a general weakening of the body`s defenses by overworking the various components of the immune system so that it is increasingly less able to respond to each new invader that comes along.

It may also be the case that helper T cells already engaged in battle against another disease are more easily infected by HIV, since the chance that they will come into contact with a wandering HIV molecule are dramatically increased.

Finally, very recent research also shows that some of the intercurrent infections common to pre-AIDS patients not only leave the immune system more vulnerable to attack but actually help the AIDS virus to reproduce itself once inside the body of the host.

In laboratory test tubes at least, the virus does not replicate inside a resting helper T cell. But when the T cell is stimulated with the same biochemical warning signals produced by the ``scout`` cells in response to an invasion, it reproduces rapidly.

``Why? We don`t know,`` admits Helga Rubsamen Weigman of Germany`s Paul Ehrlich Institute. ``But this suggests that a patient with other viral disease may produce more HIV and get sick sooner-the cofactor theory again.``